Purpose: :
Müller glia show enhanced glycolysis during diabetes anda consequence of this metabolism is cytoplasmic elevations inthe reactive dicarbonyl methylglyoxal (MGO). MGO is a well-definedAGE precursor and many cells possess a glyoxalase enzyme system(GLO1 and GLO2) that detoxify MGO and limit AGE accumulation.Using a proteomic screening approach for MGO-derived AGEs wehave sought to establish links to AGEs and retinal Müllerglia dysfunction during diabetes. We have also over-expressedGLO-1 to determine if this could limit AGE-mediated proteinmodification in high glucose-exposed Müller glia.